Ventricular fibrillation (VF) is a cause of cardiac arrest and sudden cardiac death. During VF, the ventricular muscle contracts in a much less organized pattern than during normal sinus rhythm, so the ventricles fail to pump blood into the arteries and systemic circulation. VF is a sudden, lethal arrhythmia responsible for many deaths in the Western world, mostly brought on by ischemic heart disease. VF, which occurs in approximately 2 out of 10,000 people per year, is a medical emergency. If the arrhythmia continues for more than a few seconds, blood circulation will cease as evidenced by lack of pulse, blood pressure and respiration, and death will occur.
Despite much work, the underlying nature of VF is not completely understood. Most episodes of VF occur in diseased hearts, but other episodes occur in structurally normal hearts. Much work still has to be done to understand the mechanisms of VF.
Ventricular tachycardia (VT) is a tachyarrhythmia originating from an ectopic ventricular region, characterized by a rate typically greater than 100 beats per minute and wide QRS complexes. VT may be monomorphic, i.e., originating from a single repeating pathway with identical QRS complexes, or polymorphic, i.e., following changing pathways, with varying QRS complexes. Non-sustained VT is defined as an episode of tachycardia of less than 30 seconds duration; longer runs are considered sustained VT.
No absolute ECG criteria exist for establishing the presence of VT. However, several factors suggest VT, including the following: rate greater than 100 beats per minute (usually 150-200), wide QRS complexes (>120 ms), presence of AV dissociation, and fusion beats, which are integrated into the VT complex.
VT may develop without hemodynamic deterioration. Nevertheless, it often causes severe hemodynamic compromise and may deteriorate rapidly into VF. Therefore, this tachyarrhythmia also must be addressed swiftly to avoid morbidity or mortality.
VT is defined as three or more beats of ventricular origin in succession at a rate greater than 100 beats per minute. There are no normal-looking QRS complexes. The rhythm is usually regular, but on occasion it may be modestly irregular. The arrhythmia may be either well-tolerated or associated with grave, life-threatening hemodynamic compromise. The hemodynamic consequences of VT depend largely on the presence or absence or myocardial dysfunction (such as might result from ischemia or infarction) and on the rate of VT. AV dissociation usually is present, which means that the sinus node is depolarizing the atria in a normal manner at a rate either equal to, or slower than, the ventricular rate. Thus, sinus P waves sometimes can be recognized between QRS complexes. They bear no fixed relation to the QRS complexes unless the atrial and ventricular rates happen to be equal. Conduction from atria to ventricles is usually prevented because the AV node or ventricular conduction system is refractory due to ventricular depolarizations caused by the VT. VT is uncommon in the absence of apparent heart disease.
Myocardial infarcts heal by forming scar tissue, which can lead to VT. This can occur days, months, or years after the infarction. VT can also result from anti-arrhythmic medications (an undesired effect) or from altered blood chemistries (such as low potassium or magnesium levels), pH (acid-base) changes, or insufficient oxygenation.
Fast atrial arrhythmias such as atrial fibrillation (AF) and atrial tachycardia (AT) are abnormal heart rhythms which afflict around three million people each year in the United States. The most prevalent electrical manifestation of the disease electrically is a preponderance of irregular AF wavelets of activation. These irregular AF wavelets are frequently generated in the pulmonary veins (PVs) and are conducted into the left atrium and then the right atrium, causing chaotic and rapid activation that interferes with the normal sino-atrial and atrio-ventricular (SA/AV) node cardiac electrical pathways and generates rapid, irregular ventricular contractions. These irregular AF wavelets can be in the form of AF or atrial flutters, typical and atypical, which may vary in terms of severity and rate. AF makes the ventricular response so irregular and fast that it interferes with normal blood flow through the heart chambers, can lead to severe structural heart disease, and can be life-threatening if not treated effectively. While the irregular rate of ventricular contraction during AF and AT may compromise cardiac output and cause fatigue, much of the increased mortality associated with AF is due to clot formation resulting from poor circulation in the atria that embolizes to cause stroke, renal infarcts, etc. Persistent AF over weeks or months is particularly dangerous.
A procedure to treat AF or AT is DC cardioversion shock therapy to convert AF/flutter to sinus rhythm. This is an excellent conversion tool; however, unless the underlying cause of the AF is resolved, it most likely will recur. Implantable cardioverter defibrillators (ICDs) have been used for conversion of AF; however, since the patient is conscious when the shock is delivered, many individuals find the discomfort of the shock intolerable.
Modern ICDs operate basically by using a high voltage capacitor discharge which consists of four IGBT or MOSFET saturated switches in an H-bridge configuration which produces biphasic truncated exponential (BTE) waveforms. This consists of a phase 1 positive pulse and a phase 2 negative pulse that makes up the BTE waveform. There are only a few manufacturers of ICDs in the world, and the BTE waveform may vary between brands. However, this would be relative to peak voltage for phase 1, the tilt angle or decay of the capacitor discharge, and the pulse-width variability of phase 1 and phase 2. The anode lead is generally inserted in the RV at the apex or most distal end of the RV heart chamber. The cathode is generally the “Hot Can” which is the ICD case.
The more sophisticated of these technologies sample the impedance as the fast leading edge of phase 1 shock is delivered through the heart. Based on the impedance calculated from the initial phase 1 shock, the microprocessor within the ICD adjusts the phase 1 pulse width which minimizes the tilt or rate of decay or discharge from the capacitors. In other words, in the depolarization phase, total pulse width is adjusted in an attempt to maintain the tilt angle of phase 1 by narrowing the pulse width to maintain as much constant energy delivery as possible.
In phase 2, known as the hyperpolarization phase, the pulse is generated by truncating or fast switching from one pair of IGBTs to the second pair which switches the remaining energy stored in the capacitor(s) negative with respect to the zero voltage crossing point. The remaining energy is delivered and usually presented by an appearance of having approximately one half the peak voltage of phase 1 and is conducting until the manufacturer decides a pre-determined pulse width time period which is adequate for hyper-polarization of the ventricular cardiac syncytium. The appearance will also present a positive tilt angle based on the decay rate of the remaining energy stored within the capacitors. Some stored voltage and energy may be remaining on the capacitor(s). Anode and cathode are swapped electrically when the voltage and current change direction between phase 1 and phase 2.
Different manufacturers have made their own calculations and their own determinations regarding phase 1 and phase 2 peak voltages and time periods.
In sum, the only dynamic, “real time” adjustments that can be made on-the-fly during a cardioversion or defibrillation shock is the ability to (1) measure the impedance of the cardiac muscle, and (2) change the phase 1 and phase 2 pulse widths in an attempt to adjust and hold up the tilt angle, particularly of phase 1, to statistically most effectively and reliably cardiovert and/or defibrillate. BTE waveforms contain a fast leading edge rise time from zero to about +600 VDC to +800 VDC. However, the remainder phase 1 and 2 waveforms are descending in nature, that is, they deliver decreasing energy with increasing time.
All of the conditions described above can be treated by defibrillation, including external defibrillation or cardioversion. There is a need for devices for delivering more appropriate waveform shocks and for improved waveform management systems.